One way in which the aging process can manifest itself at the organismal level is declining function in a number of areas, including sexual performance, metabolic efficiency and capacity, cognitive ability, and sensory dynamic range. While the bases underlying such decline is not fully understood, it is recognized that these often are due in part to age-related changes in organs and tissues. For example, age-related changes in human and rodent hearts include a reduction in the number of myocytes, myocyte hypertrophy, cardiac fibrosis, lipofuscin pigment accumulation, a reduction in calcium transport across sarcoplasmic reticulum membrane, and alterations in the response to adrenergic stimulation. Collectively, these alterations can contribute to age-related heart disease.
Such changes can in turn be a function of changes in the various cell types that make up tissues and contribute to their function in organ systems. The activity, structure, and identity of a cell arises from its specific protein complement, as regulated by gene expression. As such, age-related changes in cellular structure and function likely find a basis in changes in genetic expression. Therefore, aging can be reflected in genetic function.
Through increasingly more sophisticated methods of measuring gene expression, it has become possible to identify genetic correlates of aging. For example, the use of whole genome transcriptional profiling, DNA microarrays, and quantitative PCR (qPCR), it is possible to identify transcriptional biomarkers of aging and to quantify the effects of aging on their expression. Interventions that retard or counteract these effects can therefore be beneficial in counteracting organismal aging.